title: S-allyl cysteine attenuates oxidative stress associated cognitive impairment and neurodegeneration in mouse model of streptozotocin-induced experimental dementia of Alzheimer's type.
abstract: S-allyl cysteine (SAC), a sulfur containing amino acid derived from garlic, has been reported to have antioxidant, anti-cancer, antihepatotoxic and neurotrophic activity. This study was designed to examine the pre-treatment effects of SAC on cognitive deficits and oxidative damage in the hippocampus of intracerebroventricular streptozotocin (ICV-STZ)-infused mice. Mice pre-treated with SAC (30mg/kg) and vehicle (intraperitoneal; once daily for 15days) were bilaterally injected with ICV-STZ (2.57mg/kg body weight), whereas sham rats received the same volume of vehicle. The pre-treatment of this drug to Swiss albino mice has prevented the cognitive and neurobehavioral impairments. An increased latency and path length were observed in lesion, i.e. streptozotocin (STZ) group as compared to sham group and these were protected significantly in STZ group pre-treated with SAC. Levels of reduced glutathione (GSH) and its dependent enzymes (Glutathione peroxidase [GPx] and glutathione reductase [GR]) were decreased in STZ group as compared to sham group and pre-treatment of STZ group with SAC has protected their activities significantly. Conversely, the elevated level of thiobarbituric acid reactive substances (TBARS) in STZ group was attenuated significantly in SAC pre-treated group when compared with STZ lesioned group. Apoptotic parameters like DNA fragmentation, expression of Bcl2 and p53 were protected by the pre-treatment of SAC against STZ induced cognitive impairment. This study concludes that intervention of SAC could prevent free radicals associated deterioration of cognitive functions and neurobehavioral activities.
authors.affiliation: Neurotoxicology laboratory, Department of Medical Elementology and Toxicology (Fund for the Improvement of Science and Technology sponsored by DST and Special Assistance Programme sponsored by UGC), Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi-110062, India.
authors.forename: Hayate
authors.initials: H
authors.lastname: Javed
authors.forename: Mohd Moshahid
authors.initials: MM
authors.lastname: Khan
authors.forename: Andleeb
authors.initials: A
authors.lastname: Khan
authors.forename: Kumar
authors.initials: K
authors.lastname: Vaibhav
authors.forename: Ajmal
authors.initials: A
authors.lastname: Ahmad
authors.forename: Gulrana
authors.initials: G
authors.lastname: Khuwaja
authors.forename: Md Ejaz
authors.initials: ME
authors.lastname: Ahmed
authors.forename: Syed Shadab
authors.initials: SS
authors.lastname: Raza
authors.forename: Mohammad
authors.initials: M
authors.lastname: Ashafaq
authors.forename: Rizwana
authors.initials: R
authors.lastname: Tabassum
authors.forename: M Saeed
authors.initials: MS
authors.lastname: Siddiqui
authors.forename: O M
authors.initials: OM
authors.lastname: El-Agnaf
authors.forename: Mohammed M
authors.initials: MM
authors.lastname: Safhi
authors.forename: Fakhrul
authors.initials: F
authors.lastname: Islam
mesh_terms: D000544:Alzheimer Disease / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D003545:Cysteine / Q000031:analogs & derivatives* / Q000494:pharmacology; D004195:Disease Models, Animal; D007150:Immunohistochemistry; D007276:Injections, Intraventricular; D018782:Maze Learning / Q000187:drug effects; D051379:Mice; D009410:Nerve Degeneration / Q000517:prevention & control*; D009498:Neurotoxins / Q000008:administration & dosage / Q000633:toxicity; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D013311:Streptozocin / Q000008:administration & dosage / Q000633:toxicity
chemical_list: D000975:Antioxidants; D009498:Neurotoxins; D013311:Streptozocin; C065299:S-allylcysteine; D003545:Cysteine